Strokes, heart attacks and peripheral arterial disease - cardiovascular risk is about common and important ill health outcomes.
Any moves you make to reduce this risk, will have lots of more immediate benefits, however.
Nearly everyone feels better when they exercise and lose weight.
Common recommendations to wait until after 45 years age before assessing this risk, are made because the authorities are concerned pharmaceuticals may be prescribed when the chance of benefit is small.
Earlier assessment may however encourage us to have more years of healthier lifestyle and correction of metabolic disturbances by natural means.
If you are seeking advice on your personal cardiovascular system (CVS) risk, it is worth understanding about relative and absolute risk reduction.
If you have a very small risk of something happening, even a 50% (relative) reduction in that risk is not very important. The absolute risk reduction will also be very small.
Conversely if one's risk is high, everything matters¹².
The National Heart Foundation of New Zealand has published an absolute risk calculator which is quick and easy to use...
This is just a portion of the two page chart, which takes 6 factors into account (those shown plus gender.) One often ends up with a result between two colors, which is still quite easy to use...
The chart uses total cholesterol / HDL ratio, as this is a much better predictor of coronary artery disease risk than is the total cholesterol alone. The value of the ratio is the same in Imperial and Systeme International units.
Always make sure that a high density lipoprotein (HDL) is done whenever your cholesterol is measured.
I use the right hand figures, of the number of people in the same situation now, who would need 5 years of conventional treatment to prevent one episode of cvs illness.
As an illustration, for a 50 year old male, BP 180/105, TC/HDL ratio 8, non diabetic and non smoker, the absolute risk is 15-20%.
The NNT (number needed to treat) is 16.
Total expected events untreated is 3 (15-20% of 16,) so the figures are as seen.
Two events not prevented, one prevented and 13 people in the clear for now.
Presented with these figures, one person might say if they had one chance in 16 of winning a lottery, they would buy tickets for five years.
Another person might say that taking drugs for 5 years, with the risks and doctor visits entailed, all for one chance of benefit in 16, would not interest them.
I do point out as I present the figures, that the two episodes of illness may not have been as severe, and that the other 13 people may have not developed arterial disease as much, reducing future risk.
The benefits of various medications are commonly quoted as
percentage relative risk reductions. These don't mean much without the
above type of information.
This substance is a partial breakdown product of methionine, one of the building blocks of our proteins.
The breakdown cannot be completed nor reversed, because of lack of one of four substances needed for these jobs. The four factors are vitamins B6, 9 and 12 and betaine.
Homocysteine has the same history in medicine as cholesterol. Families were found who had very high levels due to genetic mutations, and very increased cardiovascular risk.
Increased homocysteine levels are associated with 10% of the variance in risk between middle aged males. Cholesterol accounts for a smaller proportion
Correcting the appropriate deficiency often relieves symptoms such as fatigue, balance problems and sleep disturbance. It is definitely not a case of pie in the sky...
The Cochrane Collaboration is an international organization which studies medical literature and publishes good reviews on many topics. Their most recent review on this subject, concluded that there is no evidence that reducing homocysteine with vitamins, will reduce CVS risk.
They state however..."It is interesting to mention that HOPE-2 2006 study (which showed a significant reduction of stroke) was the only study to use an adequate dose of vitamin B12."
It appears that none of the studies included, looked at whether people had Helicobactor pylori infection, which causes vit B12 and folate deficiency. Certainly none of them used injections of vitamin B12. I think the jury should still be out.
The recognition of the SNP in the gene encoding MTHFR,¹⁶ and the frequency of folate deficient diets, has distracted people from careful correction of B12 status in much of the research.
This first one uses imperial units, as in USACoronary Heart Disease Framingham Point Scores
This one uses SI units as in AustraliaFull copy of New Zealand risk calculator
The MacArthur Successful Aging Study, a longitudinal study of high-functioning men and women, average age 74, was recently reported (in the October '09 issue of the Annals of Epidemiology.)
Waist-hip ratio was found to predict all-cause mortality in these older adults.
Whether over eating and under exercising are purely habits or due to our belief systems or emotional stuff, this whole scenario often offers the greatest possibilities for useful change in our lives.
You can feel better as well as living longer, which is really more to the point.
If you're in the mood for radical change, look at "The New Raw Energy" by Leslie Kenton.
The original evidence in favour of this connection, was actually quite weak.
Evidence is now coming up after introduction of anti smoking legislation, which may be still just an association rather than cause and effect.
Never-the-less, where there's smoke there's fire. I'll keep an open mind on it, and advise people to stop smoking.
Sugar sticks to protein, at a rate dependent on the sugar level in the blood. This is measured in our haemoglobin, to monitor blood sugar levels in diabetes.
It is one of the factors which accelerate aging, and has just been shown⁶ to predict cardiovascular disease and all cause mortality in people without diabetes.
The best HbA1c was 5-5.4, with progressively more trouble as levels rose, but also higher mortality if <5%. This is an example of the "J-shaped curve" often seen, where too much or too little of something indicates trouble.
Their revised recommendations for diabetes diagnosis use hemoglobin A1c (HbA1c) as an easier diagnostic test, not requiring the 12 hours water only and two hours waiting needed for the oral glucose tolerance test (OGGT) used previously.
They hope that use of the HbA1c will encourage more people to get tested for type 2 diabetes and help further reduce the number of people who are unaware of this cardiovascular risk factor.
Type 2 diabetes actually can be prevented, as long as lifestyle changes are made while blood glucose levels are still in the pre-diabetes range."
From a large, easily digested meal, glucose and free fatty acids are absorbed too quickly to be processed normally and stimulate oxygen free radical formation.
Traditional Mediterranean and Okinawan diets were similar to the ancestral hunter-gatherer pattern - minimally processed natural food our metabolism can handle better.
A really hot topic in cardiology research is "vulnerable plaque." This "thin-cap fibroatheroma" fatty deposit in the lining of an artery, with a thin protective layer over, is thought to be more at risk of rupture and subsequent blood clot blocking the artery.
Intravascular ultrasound is being used to find ruptured plaques in people with unstable angina.
Why do plaques rupture or get surface erosion? This is one possible connection with peridontal disease, which is a known potent risk factor for heart attacks.
Gum disease can increase a general tendency to inflammation throughout our body, and can lead to dissemination of germs via our blood stream. These can then damage plaques.
And the combination of ischaemic heart disease with depression is associated with abnormal platelet activation as measured by platelet factor 4 and beta thromboglobulin tests.
Both conditions need good treatment now.
The long-running ACE study has shown too many adverse childhood events can dramatically increase CVS risk later in life.
Niki Gratrix has the questions you can use to score yourself. Dealing adequately with this can be game changing.
Over age 55, ED (not a talking horse) carries 11% 5-year CVS risk, but it carries some extra risk even in one's 30's.
In men with type 11 diabetes, it is the strongest CVS risk factor.
This can be because of otherwise subclinical (not yet causing any other symptoms) obstructive disease of the penile arteries, but is often caused by the same endothelial dysfunction (of the cells Lining our blood vessels) which contributes to artery disease in general.
N-terminal pro-brain natriuretic peptide is a mouthful, but was better than C-reactive protein (CRP) at predicting major CVS events in older men¹¹.
A striking example of this is¹⁴ the combination of low HDL cholesterol plus low glutathione peroxidase (GPX3) enzyme.
Low glutathione peroxidase was associated overall with 2.3 times the risk in people with high levels. However in people with HDL in the lower half of its range, low GPX3 had 6 times the risk of high GPX3.
The spasm of little arteries in the heart, with muscular walls (resistance vessels,) may directly induce symptoms in ischemic diseases.
This is a credible theory¹, and opens possibilities for treatment aimed at reducing the risk of spasm, such as magnesium supplements.
"The balance between the sympathetic and parasympathetic systems can be determined by the heart rate variability (HRV), which represents the variation of the intervals between heartbeats (97). Parasympathetic nerves slow heart rate and increase HRV by releasing ACh. Sympathetic nerves accelerate heart rate and decrease HRV by releasing epinephrine and norepinephrine (98, 99). Lower HRV is a predictor of cardiac morbidity and mortality (100–102)18
Reduced capacity to respond to our body's blood pressure control mechanism (baroreflex sensitivity feedback,) and low heart rate variability, after heart attacks, both indicate vagus (parasympathetic) nerve underactivity. They have been shown to be associated with substantially increased risk of subsequent sudden death.
After recovery from ventricular fibrillation (a potentially lethal disturbance of heart rhythm,) people have markedly increased cardiac sympathetic activity.
Dysfunction of the autonomic (parasympathetic and sympathetic) nerve control of the heart also increases with age.
It can be a target for nutritional and herbal support programs and a reason to meditate.
Omega-3 oil supplements reduced heart rate and increased heart rate variability in depressed patients with coronary heart disease, in one study⁷.
Heart rate recovery measured at the end of an exercise stress test is due to return of parasympathetic Vagus nerve activity. It should be a drop of 17-20 beats per minute in the first minute. A drop of 12 or less independently predicts increased mortality.
The tiny blood vessels which supply nutrition to the walls of the coronary arteries themselves, have been shown to get blocked.
This may be important in the development of plaque instability, or even the development of plaque in the first place. See³ http://www.thincs.org and http://www.ravnskov.nu/cholesterol.htm
A strong relationship has been found² between the amount of A1 β-casein consumed and heart disease mortality.
Apparently cows used to produce A2 beta casein, and still do in some areas of the world. The difference is only one amino acid, but it changes the way our body uses the milk. This genetic variant may have come from intensive dairy cattle breeding.
A2 milk - another way to reduce your cardiovascular risk.
A morning urine albumen/creatinine ratio test is a very early sign of renal damage and a useful CVS risk factor.
In terms of mortality risk, urinary albumin excretion is a better risk stratifier than traditional risk factors, such as cholesterol⁹.
A new test for chronic renal insufficiency, called cystatin C, is very useful in young to middle aged people, for cardiovascular risk stratification.
Chlamydia pneumoniae has been found in the fatty plaques from coronary arteries, and may help cause surface damage and instability.
A very good discussion of this, from 2000, is at http://qjmed.oxfordjournals.org/cgi/content/full/93/6/375
"kinesin-like protein family member 6" is one result of "a flurry of studies" linking tiny variations in our DNA called single nucleotide polymorphisms (SNPs) with risk of various diseases.
Nucleotides are the building blocks of the deoxyribonucleic acid our genes are made of. SNPs are mutations involving a different nucleotide being substituted for the usual one at just one spot in the DNA molecule. This change can alter the protein coded for by that gene.
A KIF6 variation with one amino acid altered, present in nearly 60% of the population, is associated with about 50% more heart disease or strokes.
It also tells who will respond to statin drugs⁸, and the benefits aren't related to how much a statin lowers cholesterol.
This is not surprising. The pleiotropic effects of statins (other effects than cholesterol lowering) are probably more important in reducing cardiovascular risk.
If you are considering taking an expensive drug with an unknown long term safety, it would be very nice to know ahead of time if it had much chance of helping you.
Statin drugs have overall very little chance of helping you if your absolute risk is low.
Also, before taking a statin, one should have thyroid function checked, as low thyroid can reversibly elevate cholesterol and LDL.
Pulse pressure is the increase in pressure in an artery, from each beat of the heart. Greater pulse pressure is an independent risk factor for cardiovascular disease.
Pulse pressure depends on how fast the heart ejects blood, how much blood it ejects and the elasticity of the major arteries receiving the blood.
Loss of this elasticity with age results in progressive increase in the pulse pressure at ages over 65. Systolic pressures continue to rise on average, while diastolic pressures decline.
The value from ordinary blood pressure measurement, is less than in the aorta, in people with stiff arteries (when it matters.) This is because the stiff arteries dampen the pulse wave by the time it gets to the arm.
Our brain and kidneys are not so lucky, as they are closer to the heart and have high blood flow. The pulsatile flow reaches and damages small blood vessels here.
The heart suffers as well, because the pressure wave bounces back to it too soon, while it is still ejecting blood, instead of after contraction (when it helps coronary artery blood flow.)
Measurement of arterial stiffness from pulse wave velocity or from analysis of the wrist pulse wave, is not yet mainstream medicine.
It is a case of "watch this space" but even just on spec, nutritional support of the elastic protein (elastin) synthesis by smooth muscle cells in arterial wall connective tissue , is worth considering as part of cardiovascular risk reduction.
We naturally wish to believe the best of a mixed bag of pressures, on the basis that the higher readings were just because of more stress etc.
Readings at the doctor's rooms are 5mmHg higher than at home.
It transpires, however, that the highest readings are important - damage from the hammering on the insides of our arteries is more if there are higher pressures, even if not all the time.
One study¹³ of 303 mostly elderly people who died suddenly outside hospital, found the cause of death and these creases were associated.
In deaths due to other causes, there were about equal numbers with and without creases (57 v. 51.) In cardiovascular deaths there were over three times as many people with creases as without (154 v. 41.)
Quoting from Sandorama 1979/1
"The increases death rate as a result of ischaemic heart disease in soft-water areas suggested the influence of mineral salts concentrations in the drinking water. As this increased death rate appears to comprise principally cases of sudden heart death, the metal content of the heart muscle of these cases is of particular interest."The writer then reviewed a paper¹⁷ on just that, showing diminished Mg, K and Fe plus increased Ca, compared with hearts from other deaths.
"The harmful effects of Western dietary habits, which have led to the enormous increase in the incidence of ischaemic heart disease are possibly due not so much to increased consumption of saturated fats, cholesterol and sugar but more to a concomitant deficiency of mineral salts."
I'd back it both ways, re sugar and minerals.
“Grip strength was a stronger predictor of all-cause and cardiovascular mortality than systolic blood pressure.”
1. Med Hypotheses. 1999 Sept 53(3):200-209.
2. Ischaemic heart disease, Type 1 diabetes, and cow milk A1 beta casein.
Laugesen M & Elliott R,
New Zealand Medical Journal. 2003 Jan 24;116(1168):U295
See abstract at http://www.ncbi.nlm.nih.gov/pubmed/12601419
3. "Vulnerable Plaque Formation from Obstruction of Vasa Vasorum by Homocysteinylated and Oxidized Lipoprotein Aggregates
Complexed with Microbial Remnants and LDL Autoantibodies"
Uffe Ravnskov and Kilmer S. McCully
Annals of Clinical & Laboratory Science, vol. 39, no. 1, 2009
Several studies have suggested that the Framingham Risk Score overestimates the cardiovascular risk in Japanese-American and Hispanic men, in Native American women, and in European and Asian populations.
The SCORE (Systematic Coronary Risk Evaluation) project⁴ better predicts cardiovascular risk for European patients. There are now multiple country-specific versions of the SCORE system.
It uses age, sex, total cholesterol, total cholesterol to HDL-C ratio, systolic blood pressure, and cigarette smoking. It has separate risk scores for higher risk and lower risk regions of Europe.
A nonlaboratory-based model⁵ using the same risk factors from the Framingham Heart Study but excluding high density lipoprotein cholesterol (HDL), and total cholesterol and adding body mass index, gave almost identical ability to accurately discriminate cardiovascular disease.
In my opinion this just shows the weakness of the relationship between cholesterol and heart disease.
4. Conroy RM, Pyorala K, Fitzgerald AP, et al. Estimation of ten-year risk of fatal cardiovascular disease in Europe: the SCORE project Eur Heart J 2003;24:987–1003.
5. Gaziano TA et al. Laboratory-based versus non-laboratory-based method for assessment of cardiovascular disease risk: the NHANES I follow-up study cohort Lancet 2008;371:923–31.
6. Selvin E et al. Glycated hemoglobin, diabetes, and cardiovascular risk in nondiabetic adults. N Engl J Med 2010; 362:800-811. (Analysis from the Atherosclerosis Risk in Communities (ARIC) study, after median follow up of about 14 years.)
7. Carney RM et al Effect of Omega-3 Fatty Acids on Heart Rate Variability in Depressed Patients With Coronary Heart Disease. Psychosom Med. 2010 Aug 17.
8. Li Y et al KIF6 Polymorphism as a Predictor of Risk of Coronary Events and of Clinical Event Reduction by Statin Therapy. Am J Cardiol. 2010 Oct 1;106(7):994-8
9. Matsushita K et al Chronic Kidney Disease Prognosis Consortium; Association of estimated glomerular filtration rate and albuminuria with all-cause and cardiovascular mortality in general population cohorts: a collaborative meta-analysis. Lancet. 2010;375:2073-2081.
10 Fiona Taylor et al Statins for the primary prevention of cardiovascular disease Cochrane Heart Group. Issue 1, 2011.
11. S. Goya Wannamethee et al Journal of the American College of Cardiology 58(1) June 2011 N-Terminal Pro-Brain Natriuretic Peptide Is a More Useful Predictor of Cardiovascular Disease Risk Than C-Reactive Protein in Older Men With and Without Pre-Existing Cardiovascular Disease
12 If one has already.... any cardiovascular disease; diabetes aged over 60 or with microalbuminuria ; moderate or severe chronic kidney disease; familial hypercholesterolaemia; blood pressure over 180/110; or total cholesterol over 7.5mmol/litre (290mg/dl) - risk is high.
Microalbuminuria is very small amounts of albumin protein in the urine, too little to show up on a regular dipstick test, measured by the albumin/creatinine ratio in morning specimen of urine.
13. www.ncbi.nlm.nih.gov › Journal List › Br Heart J › v.61(4); Apr 1989
16. Single nucleotide polymorphisms are mutant DNA which involves only one (nucleotide) base pair of a gene, altering a protein enough to reduce its activity.
Methylenetetrahydrofolate reductase is one such protein, and a rate-limiting enzyme at that. Reduced activity of this enzyme can be compensated for by extra substrate (folate.)
In people with this SNP, folate supplementation restores activity of their methionine cycle, reducing their elevated homocysteine.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5449450/
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